Angiotensin II Activates the Smad Pathway in Vascular Smooth Muscle Cells by a Transforming Growth Factor-β–Independent Mechanism | Zendy

Juan RodríguezVita | Zendy; Elsa SánchezLópez | Zendy; Vanesa Esteban | Zendy; Mónica Rupérez | Zendy; Jesús Egido | Zendy; Marta Ruiz–Ortega | Zendy

Open Access

Angiotensin II Activates the Smad Pathway in Vascular Smooth Muscle Cells by a Transforming Growth Factor-β–Independent Mechanism

Author(s) -

Juan RodríguezVita,

Elsa SánchezLópez,

Vanesa Esteban,

Mónica Rupérez,

Jesús Egido,

Marta Ruiz–Ortega

Publication year - 2005

Publication title -

circulation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 7.795

H-Index - 607

eISSN - 1524-4539

pISSN - 0009-7322

DOI - 10.1161/01.cir.0000165133.84978.e2

Subject(s) - smad , ctgf , angiotensin ii , vascular smooth muscle , losartan , endocrinology , medicine , transforming growth factor , mapk/erk pathway , phosphorylation , microbiology and biotechnology , growth factor , signal transduction , biology , receptor , cancer research , smooth muscle

Angiotensin II (Ang II) participates in vascular fibrosis. Transforming growth factor-beta (TGF-beta) is considered the most important fibrotic factor, and Smad proteins are essential components of the TGF-beta signaling system. Our aim was to investigate whether Ang II activates the Smad pathway in vascular cells and its potential role in fibrosis, evaluating connective tissue growth factor (CTGF) and extracellular matrix (ECM) proteins.

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